Hidden Hunger of Vitamin E among Healthy College Students: A Cross- Sectional Study.

BACKGROUND: College students may have a risk of fat-soluble vitamin deficiencies due to unhealthy dietary habits, especially for vitamin A and E. They are important members of the human antioxidant network; deficiencies of these vitamins may increase the risk of many critical diseases. OBJECTIVE: The current study was undertaken to determine the status of vitamin A and E in college students. METHODS: Healthy college students were recruited, and fasting blood samples of them were collected and used for determining serum levels of retinol and α-tocopherol by the HPLC method. RESULTS: We found that there was no vitamin A deficiency in college students. However, vitamin E deficiency existed in 34.5% of college students, especially in males. All the students had no vitamin E adequacy. In addition, our findings showed that BMI was inversely associated with serum α-- tocopherol, but not serum retinol. CONCLUSION: These results suggest that vitamin E deficiency in college students should be given more attention, and it is necessary to consider using vitamin E supplements.

Vitamin A deficiency exacerbates extrinsic atopic dermatitis development by potentiating type 2 helper T cell-type inflammation and mast cell activation.

BACKGROUND: Vitamin A deficiency (VAD) has been hypothesized to play a role in the pathophysiology of atopic dermatitis (AD). OBJECTIVE: We sought to verify whether VAD can exacerbate AD development, and explore the possible pathophysiologic mechanism. METHODS: We detected serum vitamin A (VA) concentration in different phenotypes of AD infants (intrinsic AD, iAD and extrinsic AD, eAD), and established ovalbumin (OVA) percutaneous sensitized AD model and passive cutaneous anaphylaxis (PCA) model on VAD and vitamin A supplementation (VAS) model in wild-type mice (C57BL/6) and established AD model on both normal VA (VAN) and VAD feeding mast cell deficiency mice (ckitw-sh/w-sh ). RESULTS: The average serum VA concentration of eAD was significantly lower than that of iAD, as well as healthy controls. In OVA-induced C57BL/6 mouse AD model, compared with VAN group, VAD mice manifested significantly more mast cells accumulation in the skin lesions, more severe Th2-mediated inflammation, including higher serum IgG1 and IgE levels, more IL-4, IL-13 mRNA expression in OVA-sensitized skin, and lower Th1 immune response, including lower serum IgG2a and IFN-γ mRNA expression in the skin. But there was no significant difference in the expression of IL-17 mRNA between OVA-treated skin of VAN and VAD mice. However, in OVA-induced ckitw-sh/w-sh mouse AD model, we did not find any significant differences in the above measurements between VAD and VAN group. In PCA model, VAD mice showed remarkable more blue dye leakage than that in VAN mice. Compared with VAD group, the above-mentioned inflammatory measurements in VAS group and VAN group were similar in OVA-induced AD model mice. CONCLUSIONS AND CLINICAL RELEVANCE: VAD can exacerbate extrinsic AD by augmenting Th2-mediated inflammation and mast cell activation. Therapeutic VAS can rescue VAD-aggravated eAD. It may provide a new strategy for future prevention or treatment of atopic dermatitis.

Association between maternal vitamin E status and alpha-tocopherol levels in the newborn and colostrum.

Vitamin E is important because of its antioxidant activity in situations of oxidative stress, especially postnatally. Hence, the objective was to verify whether maternal alpha-tocopherol level is associated with the alpha-tocopherol levels of the newborn and colostrum. This is a cross-sectional study of 58 women and their term newborns from a public hospital. Blood and colostrum were collected to measure alpha-tocopherol levels by high-performance liquid chromatography. Mothers with serum alpha-tocopherol levels <16.2 mmol L(-1) and newborns <11.6 mmol L(-1) were indicative of deficiency or low levels. Mothers were divided into two groups: <16.2 mmol L(-1) and those with levels ≥16.2 mmol L(-1) . The mean (95% confidence interval) serum alpha-tocopherol levels of mothers, umbilical cords and colostrum were 28 (24-32), 6 (5-8) and 39 mmol L(-1) (32-45), respectively (P < 0.001); 19% of the women and 90% of the newborns had low alpha-tocopherol levels. Maternal alpha-tocopherol level was associated with that of the umbilical cord. Newborns from mothers at risk of deficiency had low alpha-tocopherol levels (P < 0.001). Colostrum levels of vitamin E were not influenced by maternal serum. Maternal deficiency influenced the vitamin E level of the umbilical cord but does not in the colostrum, evidencing distinct transfer mechanisms via the mammary gland.

Nutritional status in children with Shwachman-diamond syndrome.

OBJECTIVE: In Shwachman-Diamond syndrome (SDS), pancreatic insufficiency can lead to malabsorption of fat-soluble vitamins and trace elements. The aim of this study was to assess the serum concentrations of vitamins A and E, zinc, copper, and selenium and their deficiencies. METHODS: This retrospective review was performed in 21 children (12 were male; median age, 7.8 years) with genetically confirmed SDS at a tertiary pediatric hospital. Pancreatic enzyme replacement therapy (PERT) and vitamin or trace elements supplements were documented. RESULTS: Twenty patients (95%) had pancreatic insufficiency receiving PERT, 10 (47%) had a combined vitamin and trace element deficiency, 6 (29%) had an isolated vitamin deficiency, and 4 (19%) had an isolated trace element deficiency. Vitamins A and E deficiency occurred in 16 (76%) and 4 (19%) of 21, respectively. Low serum selenium was found in 10 (47%), zinc deficiency in 7 (33%), and copper deficiency in 5 (24%). Eleven patients (52%) were on multivitamin supplementation, and 2 (10%) on zinc and selenium supplements. No statistical differences were found between repeated measurements for all micronutrients. CONCLUSIONS: More than 50% of the children had vitamin A and selenium deficiencies despite adequate supplementation of PERT and supplements. Micronutrients should be routinely measured in SDS patients to prevent significant complications.

Multiple vitamin deficiencies in a patient with a history of chronic alcohol excess and self-neglect in the UK.

We report a case of inadequate diet (caused by extreme self-neglect and alcohol excess) which led to chronic severe deficiencies of vitamins A, D and E. At presentation the patient had widespread follicular hyperkeratosis of the skin, keratomalacia of both eyes and a severe cognitive impairment. He responded well to treatment including high dose parenteral vitamins, but lasting impairments in his vision and cognition have caused permanent disability.

Is it necessary to assess for fat-soluble vitamin deficiencies in pediatric patients with newly diagnosed celiac disease?

BACKGROUND: The purpose of this study was to identify the frequency of fat-soluble vitamin deficiencies in children with celiac disease (CD) and to determine the value of routine testing for these deficiencies. METHODS: We conducted a retrospective medical record review of patients with a confirmed diagnosis of CD and fat-soluble vitamin levels measured at diagnosis between 1995 and 2012 at Mayo Clinic. Patients' demographics, fat-soluble vitamin levels, and pertinent clinical factors at the time of diagnosis were collected. RESULTS: Eighty-three patients were included in the final analysis: 51 girls and 32 boys, with an average age at diagnosis of 12.8 years in girls and 13.0 years in boys. The most commonly reported symptoms were abdominal pain in 49 patients and diarrhea in 30 patients. Family history of CD was reported in 32 patients. Average vitamin levels for vitamin E, 25-hydroxyvitamin D (25 (OH) D), and vitamin A were 7.5 mg/L, 32.8 ng/mL, and 334.5 µg/dL, respectively. No patients had vitamin A deficiency, 2 patients had vitamin E deficiency, and 9 patients had mild-to-moderate vitamin D deficiency (none had severe deficiency). Both patients with vitamin E deficiency were symptomatic and had complete villous atrophy. Thirty-one patients had insufficiency of 25 (OH) D, which was less than the reported frequency of vitamin D insufficiency in the general pediatric population in the United States in 2004. None of the patients were receiving vitamin supplements at the time of diagnosis. CONCLUSIONS: Fat-soluble vitamin deficiencies are uncommon in children with new diagnosis of CD. Routine measuring of fat-soluble vitamins levels may not be necessary.

Nitrogen-bisphosphonate therapy is linked to compromised coenzyme Q10 and vitamin E status in postmenopausal women.

BACKGROUND: Nitrogen-bisphosphonates (N-BPs) are the most widely used drugs for bone fragility disorders. Long-term or high-dose N-BP use is associated with unusual serious side effects such as osteonecrosis of the jaw, musculoskeletal pain, and atypical fractures of long bones. It has escaped notice that the pathway N-BPs block is central for the endogenous synthesis of coenzyme Q10, an integral enzyme of the mitochondrial respiratory chain and an important lipid-soluble antioxidant. Our objective was to assess the coenzyme Q10 and antioxidant status in relation to N-BP exposure in women with postmenopausal osteoporosis. METHODS: Seventy-one postmenopausal women (age, 73.5 ± 5.5 y) with osteoporosis and no other malignancy were included in this cross-sectional study. Seventeen were treatment naive, 27 were on oral N-BP, and 27 were on i.v. N-BP. RESULTS: Vitamin E γ-tocopherol levels (µmol/mL) were significantly reduced in N-BP users [oral, H(2) = 18.5, P = .02; i.v., H(2) = 25.2, P < .001; mean rank comparisons after Kruskal-Wallis test). Length of time (days) of N-BP exposure, but not age, was inversely associated with the coenzyme Q10/cholesterol ratio (µmol/mol) (ß = -0.27; P = .025), which was particularly low for those on i.v. N-BP (mean difference = -35.0 ± 16.9; 95% confidence interval, -65.2 to -4.9; P = .02). CONCLUSION: The degree of N-BP exposure appears related to compromised coenzyme Q10 status and vitamin E γ-tocopherol levels in postmenopausal women with osteoporosis. This phenomenon may link to certain adverse N-BP-associated effects. Confirmation of this would suggest that therapeutic supplementation could prevent or reverse certain complications of long-term N-BP therapy for at-risk individuals.

Urinary α-carboxyethyl hydroxychroman can be used as a predictor of α-tocopherol adequacy, as demonstrated in the Energetics Study.

BACKGROUND: Other than the in vitro erythrocyte hemolysis test, no valid biomarkers of vitamin E status currently exist. OBJECTIVE: We hypothesized that the urinary vitamin E metabolite α-carboxyethyl hydroxychroman (α-CEHC) could serve as a biomarker. DESIGN: The relations between urinary α-CEHC, plasma α-tocopherol, and vitamin E intakes were assessed by using a previously validated multipass, Web-based, 24-h self-administered dietary recall, and we concurrently collected plasma and 24-h urine samples from 233 participants of both sexes. RESULTS: Median vitamin E intakes were 9.7 mg α-tocopherol/d. Intakes were correlated with plasma α-tocopherol (R = 0.40, P < 0.001) and urinary α-CEHC (R = 0.42, P < 0.001); these correlations were essentially unchanged after multivariate adjustments. On the basis of multiple regression analysis, urinary α-CEHC excretion increased by ~0.086 µmol/g creatinine (95% CI: 0.047, 0.125) for every 1-mg (2.3-µmol) increase in dietary α-tocopherol. Urinary α-CEHC excretion remained at a plateau (median: 1.39 µmol/g creatinine) until dietary intakes of α-tocopherol exceeded 9 mg α-tocopherol/d. The inflection point at which vitamin E metabolism increased was estimated to be at an intake of 12.8 mg α-tocopherol/d. Daily excretion of >1.39 µmol α-CEHC/g creatinine is associated with a greater than adequate α-tocopherol status, as evidenced by increased vitamin E metabolism and excretion. CONCLUSION: Thus, urinary α-CEHC is a valid biomarker of α-tocopherol status that can be used to set a value for the Estimated Adequate Requirement of vitamin E.

Evaluation of epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses.

OBJECTIVE: To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm. DESIGN: Prospective case series. Animals-148 horses. PROCEDURES: Neurologic, pathological, and toxicological evaluations were completed in selected neurologically affected horses over a 2-year period. Descriptive statistical analysis was performed. RESULTS: 87 QHs and 1 QH-crossbred horse were affected. Most (50/88 [56.8%]) affected horses were 1 to 2 years old (median age, 2 years [range, 2 months to 34 years]). Neurologic deficits included obtundation (53/88 [60%] horses), decreased to absent menace response (33/88 [37.5%]), proprioceptive positioning deficits, wide-based stance, ataxia, and dysmetria (88/88 [100%]). Most (78/88 [88.6%]) horses had mild ataxia, but some (10/88 [11.4%]) had moderate to severe ataxia. Low serum concentrations of vitamin E (≤ 2 mg/L) were detected in 3 index case horses and 16 of 17 randomly selected horses (13/14 affected and 3/3 unaffected) during study year 1. Dietary vitamin E supplementation did not improve neurologic deficits in affected horses; vitamin E administration in pregnant mares appeared to decrease but not prevent disease development among offspring born the following year. Lesions detected at necropsy included bilaterally symmetric neuroaxonal degeneration with axonal spheroids in the nucleus gracilis, nucleus cuneatus medialis, nucleus cuneatus lateralis, and nucleus thoracicus (5/5 horses). CONCLUSIONS AND CLINICAL RELEVANCE: Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.

Vitamin A and E status in very low birth weight infants.

OBJECTIVE: To determine vitamin A and vitamin E status in very low birth weight (VLBW) infants at the time of birth (TB), at the time of full feeding (TFF) and at term postmenstrual age (TT). STUDY DESIGN: An observational study was conducted in VLBW infants. Plasma retinol and α-tocopherol levels were measured at TB, TFF and TT. Multivitamin supplementation was given to all infants to meet the daily requirement. RESULT: A total of 35 infants were enrolled. The median (interquartile range) of gestational age and birth weight was 30 (28 to 32) weeks and 1157 g (982 to 1406 g). The median of vitamin A and vitamin E intakes from TFF to TT was 832 and 5.5 IU kg(-1) day(-1), respectively. Vitamin A deficiency occurred in 67.7% at birth, 51.6% at TFF and 82.1% at TT. Vitamin E deficiency occurred in 77.4% at birth, 16.1% at TFF and 35.7% at TT. Small-for-gestational age was the only risk factor for vitamin A deficiency. Lower amount of breast milk consumption was associated with higher incidence of vitamin E deficiency. No differences in vitamin A- or vitamin E-related morbidities between infants with and without vitamin deficiencies were found. CONCLUSION: High prevalence of vitamin A and vitamin E deficiency was found in VLBW infants starting from birth to term postmenstrual age. Therefore, a higher dose of vitamin supplementation is required.

Epilepsy in a patient with ataxia caused by vitamin E deficiency.

Ataxia due to vitamin E deficiency is important because disease progression can be stopped by supplementary therapy. A limited number of studies and case series suggest that the disease is mainly confined to the cerebellum and spinal cord tract and seems to be more common in North African countries. We report a patient from North Norway with progressive ataxia from the age of 5, bilateral dropfoot, Babinski's sign, dysarthria and early epilepsy. Two mutations, 513insTT and p.Arg134x, were detected. When treatment was initiated 25 years after onset of symptoms, the patient was bound to the wheel chair. No further progression of pareses, ataxia or epileptic seizures has been observed in a 3-year follow-up period. This case indicates that cerebral involvement may be present in patients with a lack of vitamin E. If this observation is confirmed, a further exploration of clinical presentation, anatomic involvement and geographic distribution of the disease is warranted.

Ataxia with vitamin E deficiency: update of molecular diagnosis.

Ataxia with vitamin E deficiency (AVED) is a rare autosomal recessive neurodegenerative disease, due to mutations in TTPA gene (Arita et al. in Biochem J 306(Pt. 2):437-443, 1995; Hentati et al. in Ann Neurol 39:295-300, 1996), which encodes for alpha-TTP, a cytosolic liver protein that is presumed to function in the intracellular transport of alpha-tocopherol. This disease is characterized clinically by symptoms with often striking resemblance to those of Friedreich ataxia. The neurological symptoms include ataxia, dysarthria, hyporeflexia, and decreased vibration sense, sometimes associated with cardiomyopathy and retinitis pigmentosa (Mariotti et al. in Neurol Sci 25:130-137, 2004). Vitamin E supplementation improves symptoms and prevents disease progress (Doria-Lamba et al. in Eur J Pediatr 165(7):494-495, 2006). Over 20 mutations have been identified in patients with AVED. In the present paper we summarize the recent findings on molecular genetic of this disease including the list of the known mutations.

Nutritional deficiencies during normal growth.

Nutritional deficiencies have always been a major consideration in pediatrics. Although the classic forms of many of the well-documented nutritional deficiencies are memorized during training as a physician, nutritional deficiencies that can occur in otherwise asymptomatic normally growing children are often overlooked. The two most common deficiencies seen in children who are growing normally are iron and vitamin D deficiencies. These deficiencies are surprisingly common and can have a significant impact on the overall health of a child. This article reviews these nutritional deficiencies and other less commonly seen deficiencies in children who are otherwise growing normally.

Status of selenium, vitamin E, and vitamin A among Saudi adults: potential links with common endemic diseases.

This study was designed to determine the status of selenium, dl-alpha-tocopherol, and all-trans-retinol in adults living in Al-Kharj district using serum and toenail samples, and to look for possible association between these parameters and the etiology of endemic diseases in the same area. For this purpose, we examined a cross section of samples of 743 healthy Saudi adults on routine visits to the Primary Health Care Unites (PHCUs) for different common health problems. The arithmetic mean for selenium, dl-alpha-tocopherol, and all-trans-retinol in serum and toenail selenium levels were 107.045 +/- 23.045 microg/l (n = 743, range 52.600-210.120 microg/l), 1.053 +/- 0.324 mg/dl (n = 737, range 0.29-3.42 mg/dl), 52.561 +/- 25.671 microg/dl (n = 743, range 11.20-400.85 microg/dl), and 0.634 +/- 0.221 microg/g (n = 691, range < DL - 1.797 microg/g), respectively. The average serum selenium concentration seems to be satisfactory and compares favourably with high selenium intake countries. Although none of our participants exhibited serum selenium deficiency (< 45 microg/l), 41% of our participants had toenail selenium < 0.56 microg/g reported low levels in the previous study. The mean serum dl-alpha-tocopherol concentrations fall within the upper limit of the normal range of > 0.698-1.981 mg/dl for alpha-tocopherol as found in previous studies. On the other hand, the mean serum all-trans-retinol is higher than the normal range (20-30 microg/dl). None had exhausted retinol stores trans-retinol and MDA levels in the serum was found as a sign of peroxidative lipid damage, confirming the role of vitamin A in reducing oxidative stress. Our data also revealed a link between the status of selenium, dl-alpha-tocopherol and all-trans-retinol and a number of health problems. However, these observations need larger epidemiological studies for further confirmation.

Nonsupplemented children of Latino immigrants have low vitamin E intakes and plasma concentrations and normal vitamin C, selenium, and carotenoid intakes and plasma concentrations.

OBJECTIVE: This study sought to determine and evaluate the intakes and plasma concentrations of vitamin E (alpha-tocopherol), gamma-tocopherol, vitamin C, selenium, and carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein/zeaxanthin, and lycopene) of nonsupplemented boys and girls, 4 to 8 years old, of Latino immigrants living in rural Nebraska. DESIGN: Dietary intakes of the Latino children were estimated. Their plasma samples (fasting) were analyzed for vitamin E, vitamin C, selenium, and carotenoid concentrations. Data were evaluated by sex. SUBJECTS: The subjects were a convenience sample of 4- to 8-year-old (n=29), apparently healthy, nonsupplemented children of Latino immigrants living in rural Nebraska. STATISTICAL ANALYSIS: Sex differences in parameter values were determined using general linear models; Pearson r was used for determining correlations. RESULTS: No significant differences in parameter values were observed by sex, with the exception of plasma lutein/zeaxanthin concentration. The majority (69%) had plasma vitamin E (alpha-tocopherol) concentrations<0.516 mg/dL (12 micromol/L), which is indicative of vitamin E inadequacy, and over half (59%) reported consuming less than the Estimated Average Requirement for vitamin E. All subjects had plasma vitamin C and selenium concentrations indicative of adequacy (>0.41 mg/dL or >23 micromol/L, and >6.32 microg/dL or >0.8 micromol/L, respectively), and consumed at least the Recommended Dietary Allowances for these nutrients. The plasma carotenoid concentrations of the children may be useful as norms. CONCLUSIONS: These children of Latino immigrants who did not take supplements had low plasma vitamin E (alpha-tocopherol) concentrations but normal plasma vitamin C and selenium concentrations. IMPLICATIONS: Dietetics professionals and others involved in health care need to work with Latino immigrant parents so that their children consume adequate amounts of vitamin E.

Functional Vitamin E deficiency in ApoE4 patients with Alzheimer's disease.

Oxidative stress has been implicated in the development of Alzheimer's disease (AD). Consequently, antioxidant therapies including Vitamin E (VitE) supplementation for both prevention and treatment of neurodegenerative diseases currently appears to be a promising avenue of research. The aim of the present study was to examine the relationship between AD and the ApoE phenotype, lipid parameters and VitE levels in a large cohort of elderly subjects. No absolute deficit was observed in plasma VitE levels. However in AD, ApoE4 is not associated with an increase in total cholesterol (TC) and VitE levels. Moreover, our results suggest that oxidative stress-induced injury and protection by VitE in AD are related to the ApoE phenotype. Our study strongly supports the hypothesis of an impairment of lipophilic antioxidant delivery to neuronal cells in AD leading to a tissular antioxidant deficiency which could facilitate oxidative stress.

Delayed onset of ataxia in a patient with short bowel syndrome: a case of vitamin E deficiency.

Chronic gastrointestinal disease can result in nutritional deficiencies that can have a direct effect on the neurologic system. Although acute abnormalities can be corrected, symptoms are rarely reversible. Recognizing the appropriate abnormality is a crucial part of long-term treatment strategies in this population. Because motor and cerebellar symptoms can contribute to poor feeding, aggressive supplementation should begin as soon as symptoms are recognized. We present a patient with delayed onset and progressive hypovitaminosis E and briefly review diagnostic and therapeutic options.

Ataxia with isolated vitamin E deficiency: neurological phenotype, clinical follow-up and novel mutations in TTPA gene in Italian families.

Ataxia with vitamin E deficiency (AVED) is a rare autosomal recessive neurodegenerative disorder due to mutations in the alpha-tocopherol transfer protein (TTPA) gene on chromosome 8q13. AVED patients have progressive spinocerebellar symptoms and markedly reduced plasma levels of vitamin E. We studied neurological phenotype at diagnosis, and long-term effect of vitamin E supplementation in 16 patients from 12 Italian families. The most common mutations were the 744delA and 513insTT. Two novel TTPA mutations were identified: a severe truncating mutation (219insAT) in a homozygous patient, and a Gly246Arg missense mutation (G246R) in a compound heterozygous patient. The missense mutation was associated with a mild and slowly progressive form of the disease. Vitamin E supplementation therapy allowed a stabilization of the neurological conditions in most of the patients. However, development of spasticity and retinitis pigmentosa was noted in a few patients during therapy. Prompt genetic characterization of AVED patients may allow an effective early treatment and an adequate genetic counseling.

Myoclonic dystonia as unique presentation of isolated vitamin E deficiency in a young patient.

We describe a young patient affected by vitamin E deficiency with mutation in the tocopherol transfer protein alleles and the unique presentation as myoclonic dystonia, which was practically the only symptom for 6 years before ataxia became evident. Vitamin E supplementation markedly improved both symptoms. This unusual clinical phenotype must be considered, because isolated vitamin E deficiency is eminently treatable.